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. 2012 Feb 15;9:16. doi: 10.1186/1742-4690-9-16

Figure 3.

Figure 3

Minocycline inhibited TNF-α expression and IL-1β release in patients with HAM/TSP. (A) Dose-dependent inhibitory effects of minocycline on TNF-α expressions in CD14+ cells (closed bar) and CD4+ T cells (opened bar) of HAM/TSP patients (n = 6). The PBMCs were cultured with 0, 5 and 10 μM of minocycline for 24 hours. The frequency of CD14+ cells expressing TNF-α was significantly inhibited at 10 μM of minocycline treatment in HAM/TSP patients (p = 0.0313; Wilcoxon matched-pairs signed rank test). Error bars represent SD. (B) Inhibition of IL-1β release in PBMC culture supernatants of HAM/TSP patients by 10 μM of minocycline after culture for 24 hours (n = 8). The release of IL-1β from these cultured HAM/TSP PBMCs was significantly inhibited by minocycline treatment (p = 0.0078; Wilcoxon matched-pairs signed rank test). (C) Inhibitory effects of minocycline on spontaneous lymphoproliferation in HAM/TSP patients. The PBMCs from two HAM/TSP patients (HAM#1 and #2) were cultured with 0, 2.5, 5 and 10 μM of minocycline, and pulsed with 1 μCi [3H] thymidine for 4 hours at 3 days (closed circle), 4 days (closed square) and 5 days (closed triangle). The average cpm from each well in triplicate was plotted.